Imaging of amyloid β in Alzheimerʹs disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism

Summary Background Amyloid-β (Aβ) plaque formation is a hallmark of Alzheimerʹs disease (AD) and precedes the onset of dementia. Aβ imaging should allow earlier diagnosis, but clinical application is hindered by the short decay half-life of current Aβ-specific ligands. 18F-BAY94-9172 is an Aβ ligand that, due to the half-life of 18F, is suitable for clinical use. We thus studied the effectiveness of this ligand in identifying patients with AD. Methods 15 patients with mild AD, 15 healthy elderly controls, and five individuals with frontotemporal lobar degeneration (FTLD) were studied. 18F-BAY94-9172 binding was quantified by use of the standardised uptake value ratio (SUVR), which was calculated for the neocortex by use of the cerebellum as reference region. SUVR images were visually rated as normal or AD. Findings 18F-BAY94-9172 binding matched the reported post-mortem distribution of Aβ plaques. All AD patients showed widespread neocortical binding, which was greater in the precuneus/posterior cingulate and frontal cortex than in the lateral temporal and parietal cortex. There was relative sparing of sensorimotor, occipital, and medial temporal cortex. Healthy controls and FTLD patients showed only white-matter binding, although three controls and one FTLD patient had mild uptake in frontal and precuneus cortex. At 90–120 min after injection, higher neocortical SUVR was observed in AD patients (2•0 [SD 0•3]) than in healthy controls (1•3 [SD 0•2]; p<0•0001) or FTLD patients (1•2 [SD 0•2]; p=0•009). Visual interpretation was 100% sensitive and 90% specific for detection of AD. Interpretation 18F-BAY94-9172 PET discriminates between AD and FTLD or healthy controls and might facilitate integration of Aβ imaging into clinical practice